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PubMed1973

Lymphoblastic response to autologous colon epithelial cells in ulcerative colitis in vitro.

The blastic transformation in vitro of peripheral blood lymphocytes was measured by the 72-hour uptake of tritiated thymidine ((3)H-6-thymidine) in 23 patients with mucosal ulcerative colitis, three patients with acute Crohn's colitis with rectal involvement, and seven normal subjects. The 23 patients with ulcerative colitis were subdivided into three groups, graded according to severity into seven with acute, severe, nine with active, chronic, and seven with quiescent disease. In the control cultures of lymphocytes without any added potential stimulant the uptake of (3)H-6-thymidine in the clinical subgroup of seven patients with acute, severe ulcerative colitis was significantly greater than in seven normal subjects (p<0.01). This contrasted with a reduced uptake of (3)H-6-thymidine by lymphocytes from seven patients with acute severe colitis when compared with seven normal subjects after stimulation with phytohaemagglutinin-P (PHA-P) (p<0.01). In further duplicate cultures of lymphocytes specifically stimulated by an equal number of viable autologous rectal epithelial cells, the uptake of (3)H-6-thymidine was significantly greater in seven patients with acute severe colitis when compared with seven normal subjects (p<0.01). The results in three patients with acute Crohn's colitis with rectal involvement showed no such evidence of lymphocyte sensitivity to autologous rectal epithelial cells and their uptake of (3)H-6-thymidine lay within the normal range.Evidence that the degree of lymphoblastic transformation was related to the clinical severity of ulcerative colitis was provided by the results obtained in the unstimulated and epithelial cell stimulant cultures. The uptake of (3)H-6-thymidine was directly related to the clinical severity of ulcerative colitis in the three subgroups studied. In addition, four of the seven patients with acute severe colitis were studied later in clinical remission. They were then found to have a significantly reduced uptake of (3)H-6-thymidine in response to autologous rectal epithelial cells (p < 0.01).

Acute Disease↗
PubMed1983

Increased sister-chromatid exchange frequency in patients receiving sulphasalazine therapy for ulcerative colitis.

Sister-chromatid exchange and micronucleus frequencies are reported for lymphocytes cultured in vitro from 15 patients receiving sulphasalazine therapy for ulcerative colitis and 15 controls matched for age and sex. While the patients did not differ from matched controls for micronucleus frequency there was a substantial rise in their sister-chromatid exchange frequency. This evidence of DNA damage is discussed in relation to the known cancer risk that ulcerative colitis carries and the possibility of an increased mutation rate in the germ cells of those receiving sulphasalazine therapy.

Alcohol Drinking↗
PubMedDate not supplied

[Immunohistological study of T-lymphocytes (total and helper) and B-lymphocytes of the colonic mucosa in children with Crohn's disease and non-specific ulcerative colitis].

For one to understand better the immunological mechanism in the colonic mucosae of inflammatory bowel disease, 19 children with ulcerative colitis and 12 children with Crohn's disease were studied. The inflammatory cells identified by the immunoperoxidase technique and specific markers for total T lymphocytes (CD3), helper T lymphocytes (CD4) and B lymphocytes (CD20) in differents evolutionary periods of the disease were analysed. PI (before treatment), PII (until two years of treatment) and PIII (with more than two years of treatment). In general, all marker studied in this research, presented higher averages if comparing to the control group with different degrees of significance in the different studied periods. The marker CD3, of the total T lymphocyte, increased in the epithelial (superficial and glandular) and in the lamina propria of the involved mucosae in relation to the controlled ones, was diffusely distributed over the mucosae, concentrating itself around the microgranulomas and the nodules lymphoids. In Crohn's disease, PI, its average differed significantly from the controlled ones. Similar behave was seen in the marker CD20 of the lymphocytes in the involved mucosae, whole averages were superior in relation to the controlled ones; thought, only in the PI of the Crohn's disease this difference had been significant. The immunochromatic cells CD3 distributed themselves diffusely over the involved mucosae, concentrating themselves in the interior of the lymphoides nodules and in the injured areas, near the macrophages. The marker CD4, of helper T lymphocyte also presented in the involved mucosae high averages in relation to the controlled mucosae, but without estatistic significance. The CD4 cells distributed themselves diffusely over the whole thickness of the involved mucosae, concentrating themselves around the lymphoids nodules and microgranulomas. These results confirm the participation of these elements in the pathogenesis of inflammatory bowel disease, but did not permit the establishment of any discriminatory criteria between ulcerative colitis and Crohn's disease. The results of positive correlation between the increased of CD4 and CD20 in ulcerative colitis and CD3 and CD20 in Crohn's disease show clearly the immunoregulation action of the CD4+ cells over clonal expansion and the differenciation of the B lymphocytes from plasmocytes and the IgG syntese.

Adolescent↗
PubMed2003

Budesonide treatment of collagenous colitis: a randomised, double blind, placebo controlled trial with morphometric analysis.

BACKGROUND: Collagenous colitis is characterised by diarrhoea, lymphocytic inflammation, and a thickened subepithelial collagen layer in the colorectal mucosa. No standard treatment of the disease is established. AIMS: To investigate the clinical and histological effect of oral budesonide (Entocort, AstraZeneca) in the treatment of collagenous colitis. PATIENTS: Twenty patients with collagenous colitis (collagen layer >10 micro m) and diarrhoea (>4 stools/day and/or stool weight >200 g/day). METHODS: A randomised, double blind, placebo controlled trial of budesonide treatment. Patients were randomised to placebo or budesonide for eight weeks. Stool frequency and stool weight were registered before and after treatment. Sigmoidoscopy was performed before and after treatment, and biopsies at fixed locations were obtained for morphometric analysis. RESULTS: Ten patients were randomised to budesonide and 10 to placebo. All 10 patients receiving budesonide had a clinical response compared with two in the placebo group (p<0.001). In the budesonide group, stool weight was reduced from 574 g/day to 200 g/day and stool frequency was reduced from 6.2/day to 1.9/day (p<0.01). The histological inflammation grade in the sigmoid mucosa and the thickness of the collagen layer were significantly reduced. A correlation between the grade of inflammation as well as collagen layer thickness and stool weight was found. No side effects were reported. Eight of 10 patients had relapse of symptoms within eight weeks after stopping treatment. CONCLUSIONS: Budesonide is a highly effective and well tolerated treatment of collagenous colitis. There is a high risk of relapse after stopping eight weeks of treatment.

Adult↗
PubMed1992

Microscopic colitis: can it be qualitatively and quantitatively characterized?

This study reports the histological features helpful in diagnosing microscopic colitis. Rectal biopsy specimens from 14 patients with microscopic colitis, 14 with active ulcerative colitis and 14 without colonic inflammation were pooled and then assessed by three observers according to a predetermined protocol. Inter-observer agreement was good except for Paneth cell metaplasia and endocrine cell metaplasia. Compared with healthy tissue, microscopic colitis showed a significant (p less than 0.05) increase in chronic inflammatory cells and a depletion of goblet cells but these changes were less pronounced than those seen in ulcerative colitis (p less than 0.05). In contrast to ulcerative colitis, microscopic colitis was associated with a more marked infiltration with eosinophils and an increase in intra-epithelial lymphocytes. These results show that microscopic colitis can be distinguished both from normal colonic tissue and from ulcerative colitis.

Adolescent↗
PubMed1982

Characterization of immunoregulatory T cells and lymphocytophilic antibodies in ulcerative colitis: analysis with monoclonal antibodies.

Using monoclonal antibodies to the surface antigens or suppressor/cytotoxic (Anti-Leu-2a) and helper/inducer (Anti-Leu-3a) T cell subsets, we characterized peripheral lymphocytes in 27 patients with ulcerative colitis (UC) and 15 age-matched healthy controls by a fluorescence activated cell sorter. The patients with active UC had a reduced percentage (8.2 +/- 3.6%) of Anti-Leu-2a reactive subset in comparison with healthy controls (24.6 +/- 3.6%) (P less than 0.01). No significant change was found in the percentage of Anti-Leu-3a reactive T cells between the patients and the controls. Moreover, the relationship of lymphocytophilic antibodies found in the patients with UC to the T cell subsets was also examined. After a fraction of normal T cells was eliminated with treatment of the sera from patients with active UC, the percentage of T cells reactive with Anti-Leu-2a decreased from 25 to 15%, whereas the percentage of T cells reactive with Anti-Leu-3a increased from 40 to 70%. In the reciprocal study, the lymphocytophilic antibodies reacted with 80% of Leu-3a negative T cells and 65% of Leu-2a negative T cells. These results demonstrated that the lymphocytophilic antibodies found in UC patients are reactive with suppressor T cells and thus play an important role in the loss of peripheral suppressor cells in the active UC patients. The lymphocytophilic antibodies were also demonstrated to be reactive with non-helper, non-suppressor T cell subsets and some populations of helper T cells. These studies suggest the presence of immune-regulatory disturbances contributing the pathogenesis of UC.

Adult↗
PubMed2005

Colitis in mice lacking the common cytokine receptor gamma chain is mediated by IL-6-producing CD4+ T cells.

BACKGROUND & AIMS: Mice that have a truncated mutation of the common cytokine receptor gamma chain (CR gamma -/Y) are known to spontaneously develop colitis. To identify the pathologic elements responsible for triggering this localized inflammatory disease, we elucidated and characterized aberrant T cells and their enteropathogenic cytokines in CR gamma -/Y mice with colitis. METHODS: The histologic appearance, cell population, T-cell receptor V beta usage, and cytokine production of lamina propria lymphocytes were assessed. CR gamma -/Y mice were treated with anti-interleukin (IL)-6 receptor monoclonal antibody to evaluate its ability to control colitis, and splenic CD4 + T cells from the same mouse model were adoptively transferred into SCID mice to see if they spurred the appearance of colitis. RESULTS: We found marked thickening of the large intestine, an increase in crypt depth, and infiltration of the colonic lamina propria and submucosa with mononuclear cells in the euthymic CR gamma -/Y mice, but not in the athymic CR gamma -/Y mice, starting at the age of 8 weeks. Colonic CD4 + T cells with high expressions of antiapoptotic Bcl-x and Bcl-2 were found to use selected subsets (V beta 14) of T-cell receptor and to exclusively produce IL-6. Treatment of CR gamma -/Y mice with anti-IL-6 receptor monoclonal antibody prevented the formation of colitis via the induction of apoptosis in IL-6-producing CD4 + T cells. Adoptive transfer of pathologic CD4 + T cells induced colitis in the recipient SCID mice. CONCLUSIONS: Colonic IL-6-producing thymus-derived CD4 + T cells are responsible for the development of colitis in CR gamma -/Y mice.

Adoptive Transfer↗
PubMed1997

Functional expression of the eotaxin receptor CCR3 in T lymphocytes co-localizing with eosinophils.

BACKGROUND: The chemokine eotaxin is produced at sites of allergic inflammation, binds selectively to the chemokine receptor CCR3 and attracts eosinophil and basophil leukocytes, which express high numbers of this receptor. Responses of T lymphocytes to eotaxin have not been reported so far. We have investigated the expression of CCR3 in T lymphocytes and analysed the properties and in vivo distribution of T lymphocytes expressing this receptor. RESULTS: In search of chemokine receptors with selective expression in T lymphocytes, we have isolated multiple complementary DNAs (cDNAs) encoding CCR3 from a human CD4+ T-cell cDNA library. T-lymphocyte clones with selectivities for protein and non-protein antigens were analysed for expression of CCR3 and production of Th1- and Th2-type cytokines. Of 13 clones with surface CCR3, nine secreted enhanced levels of interleukin-4 and/or interleukin-5, indicating that CCR3 predominates in Th2-type lymphocytes. CCR3+ T lymphocytes readily migrated in response to eotaxin, and showed the characteristic changes in cytosolic free calcium. Immunostaining of contact dermatitis, nasal polyp and ulcerative colitis tissue showed that CCR3+ T lymphocytes are recruited together with eosinophils and, as assessed by flow cytometry, a large proportion of CD3+ cells extracted from the inflamed skin tissue were CCR3+. By contrast, CCR3+ T lymphocytes were absent from tissues that lack eosinophils, as demonstrated for normal skin and rheumatoid arthritis synovium. CONCLUSIONS: We show that T lymphocytes co-localizing with eosinophils at sites of allergic inflammation express CCR3, suggesting that eotaxin/CCR3 represents a novel mechanism of T-lymphocyte recruitment. These cells are essential in allergic inflammation, as mice lacking mature T lymphocytes were insensitive to allergen challenge. Surface CCR3 may mark a subset of T lymphocytes that induce eosinophil mobilization and activation through local production of Th2-type cytokines.

Cell Movement↗
PubMed2005

T cell-induced inflammation of the small and large intestine in immunodeficient mice.

It is well known that transfer of CD4+CD45RBhigh (naïve) T cells into syngeneic lymphocyte-deficient mice induces chronic colitis. However, no studies have reported the presence of small bowel inflammation in this T cell-dependent model. Therefore, the objective of this study was to evaluate and compare small and large bowel inflammation induced by transfer of naïve T cells into two different immunodeficient recipient mice. T and B cell-deficient recombinase activating gene 1-deficient [RAG knockout (KO)] and T cell-deficient T cell receptor-beta x T cell receptor-delta double-deficient (TCR KO) mice were reconstituted with wild-type naïve T cells and observed for signs of disease. We found that reconstituted RAG KO mice developed moderate to severe colitis and inflammation of the entire small intestine at 6-8 wk after T cell transfer. Adoptive transfer of naïve T cells into TCR KO mice induced a milder form of chronic colitis and small bowel inflammation that was confined primarily to the duodenum at 10-12 wk after T cell transfer. T helper cell 1 and macrophage-derived proinflammatory cytokine mRNA levels correlated well with the localization and severity of the chronic large and small bowel inflammation. In addition, we observed comparable homing and expansion of donor lymphocytes in the gut and secondary lymphoid tissues of both recipients. Taken together, our data demonstrate that transfer of naïve T cells into immunodeficient recipient mice induces both chronic small and large bowel inflammation and that the presence of B cells in the TCR KO recipients may play a role in regulating chronic intestinal inflammation.

Adoptive Transfer↗
PubMed2001

Differential cytokine requirements for regulation of autoimmune gastritis and colitis by CD4(+)CD25(+) T cells.

Murine autoimmune gastritis, induced by neonatal thymectomy or the injection of CD25-depleted lymphocytes into nu/nu recipients, is characterized by an inflammatory infiltrate into the gastric mucosa, parietal cell destruction and circulating anti-parietal cell antibodies. Using RAG-2(-/-)mice as recipients, we determined that the induction of disease relies on CD4(+)CD25(-)effector cells and prevention relies on CD4(+)CD25(+)regulatory cells; neither requires participation of CD8 cells or B cells. The severity of gastritis was dependent on the cytokine repertoire of CD4(+)CD25(-)effector T cells. Recipients of IL-4(-/-)T cells developed more severe gastritis and recipients of INF-gamma(-/-)T cells developed milder disease than recipients of wildtype or IL-10(-/-)effector T cells. Gastritis did not develop in the absence of IL-12. Protection from gastritis does not require either IL-4 or IL-10 because CD4(+)CD25(+)cells from IL-4(-/-)or IL-10(-/-)mice completely abrogated the disease process. CD4(+)CD25(+)cells also protected RAG-2(-/-)recipients from colitis and inhibitory activity was partially dependent on IL-10 expression. These findings highlight the critical role of CD4(+)CD25(+)regulatory T cells in protection from several autoimmune syndromes and delineate the differential contribution of IL-10 to CD4(+)CD25(+)Treg activity in the settings of gastritis and colitis.

Animals↗
PubMed1996

[Immunoglobulin heavy chain variable region(VH) genes in B cell clones producing anti-colon antibodies in ulcerative colitis].

We have established anti-colon antibodies producing B cell clones from the patient with ulcerative colitis, and analyzed the immunoglobulin heavy chain variable region (VH) gene segments of these clones using RT-PCR with VH family specific primers. VH3 family was used by all ten clones from ulcerative colitis that produced anti-colon antibodies, while various VH gene families were used by eight clones from normal controls. By nucleotide sequence analysis, two LPL clones were thought to be derived from a germ line gene segment, VH26. However, other three PBL clones were derived from 22-2B, 9-1 and 1.9-III, respectively. These results suggest the heterogeneity of the colonic antigens that autoantibodies in ulcerative colitis recognize.

Antibody-Producing Cells↗
PubMed2002

[Importance of determination of lymphocytes in intestinal mucosa biopsy specimens using flow cytometry in the evaluation of ulcerative colitis activity].

In this clinical study, we have examined 10 patients with ulcerative colitis. The study group included 5 men and 5 women. The control group consisted of 6 patients with negative colonoscopic finding performed for differential diagnosis of the dyspeptic syndrome. Patients with ulcerative colitis were divided into two groups according to the clinical pattern, macroscopic endoscopic finding, and histological examination of the bioptic specimens. The Ist group of patients with active stage of ulcerative colitis, the IInd group of patients in remission, without clinical and endoscopic signs of disease activity. We have found that from the followed markers the greatest importance lies in the determination of the standard immunologic profile of the mucosa, the determination of activating markers HLA-DR+, CD69, CD122 and CD71 on T-lymphocytes and CD69 and CD71 on B-lymphocytes. The differences between the control group and the group of patients in active stage of the disease were statistically significant. Statistical significance was also found in some of the above-mentioned parameters when comparing the group of active disease and that one in remission (CD4/CD8 ratio, HLA-DR+, CD122 on T-lymphocytes). Our results imply that the changes in the target tissue contribute to more precise assessment and follow-up of therapeutic effect in non-specific inflammatory bowel disease.

Antigens, CD↗
PubMed1995

Evidence that CD4+, but not CD8+ T cells are responsible for murine interleukin-2-deficient colitis.

Mice deficient in interleukin-2 production (IL-2null mice) develop colonic inflammation closely resembling ulcerative colitis in humans. Although this disease is marked by substantial infiltration of the colon by CD8+ and CD4+ T lymphocytes, no function has yet been assigned to these T cell subsets in the development of colitis in the IL-2null mouse. For the present study, we investigated the involvement of T lymphocytes in the onset of colitis in IL-2null mice, and examined the possible role played by cytotoxic T cells. Both lamina propria lymphocytes (LPL) and intraepithelial lymphocytes (IEL) of the colon of IL-2null mice were potently cytotoxic ex vivo in short-term redirected cytotoxic lymphocyte (CTL) assays. In contrast, colonic T cells of wild-type animals showed little or no constitutive cytotoxic T cell activity. Colonic CTL were detectable prior to the appearance of disease in IL-2null animals and CTL activity was confined to the TcR alpha beta, rather than to the TcR gamma delta IEL subset. IL-2null animals crossed with major histocompatibility complex class I-deficient mice [IL-2null x beta 2 microglobulin (beta 2mnull) mice] also developed colitis, which appeared even earlier than in most IL-2null mice. These findings suggest that neither CD8+ IEL nor LPL were causal in the onset of colitis in IL-2null animals. In IL-2null x beta 2mnull mice, an ulcerative colitis-like disease was evident from histological studies and immunohistological staining which showed very large numbers of CD4+ lymphocytes within the intestinal mucosa. Significant ex vivo killing by CD4+ T cells was observed in IL-2null x beta 2null animals, although this required an extended incubation time compared to colonic CD8+ T cells. Peripheral as well as colonic CD4+ T cells in IL-2null and IL-2null x beta 2mnull animals, were activated as judged by their cell surface phenotype (CD45RBlo, L-selectinlo and CD69+). In light of these findings, we propose that infiltrating CD4+, but not CD8+ T cells are central to the inflammation observed in the intestinal mucosa in IL-2null colitis.

Animals↗
PubMed2003

Ameliorating effect of anti-inducible costimulator monoclonal antibody in a murine model of chronic colitis.

BACKGROUND & AIMS: Inducible costimulator (ICOS)/B7RP-1 represents a newly described receptor/ligand pair involved in costimulation of T cells by antigen-presenting cells. We investigated the involvement of the ICOS/B7RP-1 interaction in the pathogenesis of colitis and the therapeutic potential of anti-ICOS monoclonal antibody (mAb) in experimental colitis METHODS: We administered anti-ICOS or anti-B7RP-1 mAb to mice with experimental colitis induced by transfer of CD4(+)CD45RB(high) T cells from normal mice into SCID mice. The ability of CD4(+)CD45RB(high) cells derived from ICOS-/- mice to induce colitis was assessed. Th2 cytokine production and apoptosis in infiltrating T cells was examined after administration of anti-ICOS mAb. RESULTS: ICOS was strongly induced on CD4(+) T cells, and B7RP-1 was expressed by macrophages in the inflamed mucosa of colitic mice. Anti-ICOS mAb, but not anti-B7RP-1, ameliorated chronic colitis when administered in prevention or therapeutic protocols. Transfer of CD4(+)CD45RB(high) T cells from ICOS-/- mice induced colitis. Treatment with anti-ICOS mAb did not enhance the production of Th2 cytokines, but a single dose of anti-ICOS mAb induced massive apoptosis of infiltrating ICOS-expressing T cells. CONCLUSIONS: ICOS/B7RP-1 interactions are not required for the development of colitis. However, treatment with anti-ICOS mAb can prevent and reverse intestinal inflammation by inducing apoptosis of ICOS-expressing T lymphocytes.

Adoptive Transfer↗
PubMed1998

Involvement of CD4+ T cells in the development of dextran sulfate sodium-induced experimental colitis and suppressive effect of IgG on their action.

1. To clarify the role of T cells in the development of dextran sulfate sodium (DSS)-induced colitis, T cells from colitis mice were primed with DSS-pulsed macrophages in vitro and then transferred into normal mice. In addition, to determine whether the target cell of immunoglobulin G (IgG) is the T cell, the extent of T cell proliferation induced by pulsed macrophages was examined after preincubation with IgG. 2. When mice receiving the primed T cells were treated with oral DSS, colitis symptoms were more severe than in animals treated with oral DSS only. This activity of primed T cells was reduced by depletion from the cells of CD4+ but not CD8+ cells. 3. The proliferation of T cells from colitis mice induced by pulsed macrophages was inhibited by T cell preincubation with homologous IgG. 4. The results suggest that CD4+ T cells play an important role in the development of DSS-induced experimental colitis and that IgG may modulate the development of colitis through interaction with pathogenic T cells.

Adoptive Transfer↗
PubMed1976

The detection of serological factors in acute ulcerative colitis indicating a favourable short-term prognosis.

Large-intestinal epithelial cells were obtained from operation specimens and by biopsy at sigmoidoscopy from 16 patients with acute severe mucosal ulcerative colitis and II control subjects with normal large-bowel mucosa. The ability of lymphocytes to release 51Cr label from large-intestinal epithelial cells was quantitatively assessed as percentage lymphocyte activity. The mean +/- standard deviation of percentage lymphocyte activity in 16 patients with acute ulcerative colitis on admission to hospital (88 +/- 8) was significantly greater than that in II normal subjects (16 +/- 8) (P is less than 0.01). In each study, samples of autologous serum were added to two reactions between lymphocytes and autologous large-intestinal epithelial cells. The results in the seven patients who came to urgent colectomy differed significantly from those in the nine who responded to corticosteroids. The mean +/- S.D. of percentage serological inhibition of lymphocyte activity in the group coming to colectomy was 44 +/- 16, and in those responding to steroids 12 +/- 5. When the serum of these patients was studied for immunofluorescent autoantibodies to normal human colonic mucosa, none of the seven patients treated by colectomy had detectable autoantibodies, in contrast with three of the nine patients with a more favourable short-term prognosis, in that they responded to steroid treatment.

Acute Disease↗
PubMed1993

Expression of CD45RO on circulating CD19+ B-cells in Crohn's disease.

Crohn's disease is an immunoregulatory disorder of the intestine that can be associated with systemic manifestations. This study analysed B-cell differentiation antigens to identify B-cell subpopulations unique to patients with Crohn's disease. CD45 isoform expression was used as an indicator of B-cell differentiation stage. This work shows that B-cells in blood and gut of patients with Crohn's disease are at an advanced stage of differentiation based on their unusual presentation of transitional (RA+ RO+) and late stage (RO+)CD45 isoforms on lamina propria lymphocytes, whereas normal intestinal lamina propria lymphocytes B-cells express primarily CD45RA. Crohn's disease patients had heightened expression of the CD45RO isoform on CD19+ lamina propria lymphocytes, and was found in a statistically significant proportion of Crohn's peripheral blood mononuclear cells (PBMC) where CD19+ PBMC had an expression pattern affecting an unexpectedly high proportion of these differentiated or late stage CD45RO+ B-cells. The expression of CD45RO varied greatly among CD19+ PBMC from patients with Crohn's disease, so multiple regression analysis was performed between these CD45 isoforms and several clinical parameters. After grouping high and low CD45RO expression on CD19+ B-cells, a significant statistical difference was found between high Crohn's disease activity index (CDAI) and low CDAI Crohn's disease patients respectively.

Antigens, CD↗